Pericardial effusion in hypothyroidism is common. But an effusion which causes cardiac tamponade is a rarity.[9] We report below one case with myxedema and cardiac tamponade due to pericardial effusion.

M.R.P., a 40 year old male was admitted with progressive distension of the abdomen, puffiness of the face, edema of feet and exertional dyspnoea, all of six months' duration. His skin had thickened and become coarse over this period, and he had been treated as a case of pellagra by his family physician. There was no history of paroxysmal nocturnal dyspnoea, orthopnoea, oliguria" chest pain, syncope or palpitation. The patient had been an alcoholic for five years and smoked about five cigarettes per day. There was no past history to suggest ischemic heart disease, diabetes mellitus or hypertension. He had been treated ten years earlier for "serpent like" skin with some tablets, which he had stopped two years ago.On examination, the patient was averagely built and nourished and had thick, slow speech. His axillary temperature was 370C. The pulse was slow (60/min.), regular, of low volume and showed pulsus paradoxus. The blood pressure was 90/70 mm of Hg. The jugular venous pressure was raised upto the angle of the jaw, no waves being discernible. His face was puffed up, more so the eyelids. He had a sallow complexion and loss of lateral third of the eyebrows. The skin was dry and coarse all over, with areas of lichenification around the umbilicus and on the dorsum of both feet. The cardiac apical impulse was not visible. The apex beat was not felt. On auscultation, the heart sounds were distant. There was no murmur. there were a few crepitations at both the lung bases. There were branding marks over the abdomen. The liver was palpable five cm below the costal margin, firm and nontender, with a smooth surface and a sharp border. The spleen was not palpable. There were signs of free fluid in the abdomen. His deep reflexes showed delayed relaxation.InvestigationsHaemoglobin: 13.8 gm%, PCV: 44%, WBC: 6,500/cmm, with P: 62%, E: 4%, L: 34%, ESR: 6 mm/hr., Urine, stool, renal chemistry, liver function tests and blood glucose were normal. The ascitic fluid was yellow in colour, opalescent and had a fibrin clot; it had 70 lymphocytes per cmm. a few mesothelial cells, and 3.72 g% of protein. Eight hundred and fifty ml of pericardial fluid was removed; it was yellow and opalescent ("Gold Paint" effusion), contained fibrin. RBCs, lymphocytes (20/cmm), proteins: 4.74 g%, and cholesterol: 176 mg%; no organisms were grown on culture. X-ray chest (PA view) revealed gross cardiomegaly [Fig. 1]. E.C.G. showed sinus bradycardia, low QRS voltage, and flat T waves all over [Fig. 2] Echocardiogram showed a large pericardial effusion both in the anterior and inferior recesses. LV echoes displayed findings indicative of cardiac tamponade. These included synchronous septal and LV endocardial motion and phasic variation in mitral opening amplitude in respective frequency. Mitral EF slope was normal. Cavity dimensions were normal. Thyroid function tests showed T3 charcoal uptake of 65% (Normal: 84-116%); radioactive iodine uptake at 4 hours was 4 % and at 48 hours 1%. Radio immunoassay of T4 and TSH showed levels of 1.4 ug/100 ml. (Normal: 5-12 pg/100 ml) and 40 u units per ml (Normal: < 6 uU/ml) respectively.The patient's symptoms were relieved after the pericardial tapping. A repeat X-ray chest showed that the heart size was now well within normal limits. The voltage of the E.C G. showed some improvement [Fig. 2] The repeat echocardiogram showed no evidence of cardiac tamponade. The earlier findings in regard to mitral opening peak and the heart swing were absent. There was evidence of a small effusion in the deep inferior and the anterior recesses of the pericardium (as shown by systolic separation only), though clearly of a lesser degree.The patient was treated with I-thyroxine sodium 0.1 mg daily which was later increased gradually to 0.2 mg daily. Within a few weeks, all his symptoms and signs disappeared and he became normal.

Myxedema heart disease as a distinct entity was first described by Zondek[10] in 1918 and defined completely by Fahr[4] in 1925. Kern et al[5] described pericardial effusion as a "constant, early and major factor in myxedema heart." Its presentation is similar to that of congestive cardiac failure. The pathophysiologic derangements responsible for the collection of fluid in the serous cavities of myxedema patients are probably increased systemic capillary permeability[6] and disturbances in electrolyte metabolism.[7]The rarity of cardiac tamponade[2], [8], [9] in myxedema patients with pericardial effusion is attributed to the slow accumulation of fluid and the remarkable distensibility of the pericardium. The pericardial fluid is straw coloured with specific gravity between 1012 and 1025. It has a high content of alpha and beta globulins, white blood cells, mainly polymorphs and red blood cells, the latter from the fragile capillaries.Alexander[1] first used the term "Gold Paint Effusion" to describe the golden brown appearance of the pericardial fluid due to the shimmering satin cholesterol crystals. The high cholesterol content of the fluid has been attributed to disturbances in lipid meabolism;[3] possibly a churning action of the heart plays a role in the precipitation of cholesterol from pericardial fluid or the poor absorptive capacity of the pericardium may be a major factor.